The majority of cholesterol entering the intestinal tract is biliary cholesterol. Biliary cholesterol secretion averages 1000 mg per day as part of the bile system and enters as free cholesterol already solubilized with bile acids and phospholipids. Both cholesterol absorption by enterocyte and biliary cholesterol secretion by hepatic cells are regulated by expression of the half-transporters ABCG5 and ABCG8. Studies in animals have shown that treatment with a LXR agonist decreases cholesterol absorption, increases biliary cholesterol secretion, and increases fecal neutral sterol excretion. Studies in transgenic mouse models demonstrate that increased expression of ABCG5 and ABCG8 increases biliary neutral sterol secretion and reduces intestinal cholesterol absorption, leading to increased neutral sterol excretion and cholesterol synthesis.
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